The formation of a collagenous scar in the vitreous with its contraction and tension on the retina is a well-known but poorly understood complication of numerous ocular diseases. Normal collagen in human vitreous consists of a unique type of ((a1)11)3 molecule in the form of very thin filaments which presumably contributes to its optical transparency and gel-like consistency. It is hypothesized here that injury to the vitreous stimulates production of a different type of collagen, which is able either to condense into thicker fibers, or to undergo more extensive cross-linkage accounting for marked contraction vitreous scar tissue. Vitreous hemorrhage containing Fe ion, hemoglobin and inflammatory cells likely leads to a peroxidative depolymerization of the hyaluronate-protein complex which in turn acts as a major stimulus to the formation of abnormal collagen. This hypothesis will be tested by assaying various morphologic and metabolic characteristics of normal and traumatized vitreous including: rate of collagen synthesis, activity of prolyl hydroxylase, lysyl oxidase, and chemical composition of the various types of collagen, collagen filaments, scanning EM of collagen orientation, and routine histochemical studies of fibrous tissues and scars in three experimental animal models designed to stimulate as closely as possible the pathogenesis and pathology of vitreous reactions among clinical disorders. Beta-aminopropionitrile (BAPN), an inhibitor of lysyl oxidase, will be used in the form of large molecular weight BAPN-polymer to block the formation of cross-linkage in newly formed vitreous collagen and antioxidants or free radical scavengers (vit. E (superoxide dismutase)) will be used to inhibit peroxidation.